Is there an optimal degree of acid suppression for healing of duodenal ulcers?

Burget, D. W.; Chiverton, S. G.; Hunt, Richard H.

doi:10.1016/0016-5085(90)91015-x

Cited by 311 publications

(57 citation statements)

References 13 publications

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“…These data confirm the inhibitory effects of omeprazole on acid secretion, although, in this study, pH exceeded 4.0 for about 48–50% of the recording in the distal corpus compared with duration of 64% reported by Burget et al [1]. This may reflect intrinsic interindividual variability in response to omeprazole, but it is possible that the higher values in previous studies are due to the inclusion of subjects with H. pylori infection [21, 22, 23, 24].…”

Section: Discussionsupporting

confidence: 71%

“…The healing rates achieved by acid antisecretory agents in peptic ulcer disease and reflux esophagitis correlate with their ability to reduce gastric acidity [1, 2, 3]. However, there is continuing debate as to the optimal level of acid suppression that will produce healing and maintain remission in reflux oesophagitis [1, 3, 4].…”

Section: Introductionmentioning

confidence: 99%

“…However, there is continuing debate as to the optimal level of acid suppression that will produce healing and maintain remission in reflux oesophagitis [1, 3, 4]. At currently recommended doses, omeprazole produces a greater reduction in gastric acidity than the histamine H 2 -receptor antagonists [1, 2, 3, 5].…”

Section: Introductionmentioning

confidence: 99%

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Effect of Omeprazole on Regional and Temporal Variations in Intragastric Acidity

Viani

Verdú²,

Idström³

et al. 2002

Digestion

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Background: Conventional techniques for measuring gastric acidity have demonstrated the decrease in gastric acidity produced by proton pump inhibitors (PPI); however, such techniques do not detect transient or localized pH changes which may modify the intragastric environment without affecting the therapeutic efficacy of PPIs. Aim: To investigate local and temporal variations in intragastric pH and to test the hypothesis that omeprazole produces prolonged, generalized gastric anacidity (pH >6). Methods: A single-blind study was conducted with triple-point 24-hour gastric pH-metry on days 7, 14 and 21 in 14 healthy, Helicobacter pylori-negative volunteers (7 M; 20–46 years) who received placebo for 7 days, followed by omeprazole 20 mg daily for 14 days. Results: Omeprazole increased the median 24-hour pH significantly in the distal corpus (placebo: 1.3 (95% CI 1.1 to 1.6); omeprazole week 1: 4.0 (2.6–5.0); omeprazole week 2: 4.0 (2.8–4.6)) and at all other gastric recording sites (p < 0.01). At both corpus sites, nocturnal pH was lower and mealtime pH was higher than the non-meal daytime pH during placebo and both omeprazole administration periods; in the antrum, however, the major difference noted was that meal-time pH was higher than non-meal daytime pH. Antral pH was lower during meals and higher at night than proximal corpus pH. During placebo, gastric pH >6.0 was observed at 1 site only for 1.7% (median; 95% CI 0.4–3.3%), at 2 sites simultaneously for 0.24% (0.0–1.0%) and at 3 sites for 0.0% (0.0–0.28%), respectively, of the recording periods; during the second week of omeprazole, the equivalent results were 7.7% (1.4–14.0%), 4.9% (0.21–15.7%) and 4.7% (0.0–9.9%), respectively. Conclusions: Omeprazole, 20 mg daily, does not produce gastric anacidity despite significant increases in median 24-hour pH values. The time-, meal- and site-related variations in gastric pH observed under normal physiological conditions are seen to persist, with prolonged periods of low pH throughout the stomach and preservation of the normal, meal-related rise and nocturnal fall in gastric pH during omeprazole administration.

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Section: Discussionsupporting

confidence: 71%

Section: Introductionmentioning

confidence: 99%

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Effect of Omeprazole on Regional and Temporal Variations in Intragastric Acidity

Viani

Verdú²,

Idström³

et al. 2002

Digestion

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“…peptic ulcer, re¯ux oesophagitis), intragastric pH should be elevated above 3 or 4 for a certain period of time (e.g. 16 h) to achieve rapid and optimal healing 20,21 and second, acid suppression is needed for the synergistic action of the concomitantly given antibiotics for eradicating H. pylori. 9,19 Thereby it remains questionable whether drug-speci®c properties or the extent and duration of acid suppression affect eradication and which patient factors contribute to the large variability.…”

Section: Discussionmentioning

confidence: 99%

Age‐dependent eradication of Helicobacter pylori with dual therapy

Treiber

Ammon

Klotz

1997

Aliment Pharmacol Ther

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A causative role is now accepted for Helicobacter pylori for the development of erosive gastritis, duodenal and gastric ulcer. Eradication of the infection results in cure of erosive gastritis and a stable remission of peptic ulcer. During the last few years different treatment regimens have been tried, of which omeprazole and amoxycillin have been the most frequently used because this dual therapy is simple (b.d. dosing for 2 weeks) and welltolerated. However, the eradication rates vary widely (10±80%) and the decisive factors in¯uencing the ef®cacy remain unclear. 1, 2Based on experience with classical triple therapy (bismuth salt + two antibiotics), age might be considered as an important factor. However, although one trial reported an association between H. pylori eradication rate and advanced age, 3 another study could not . Intragastric pH and plasma levels of the administered drugs were monitored over a dosing interval of 12 h. Results: The overall eradication rates were 45% (intention-to-treat, ITT, 27/60) or 47% (per protocol 27/58); they did not differ (ITT) between omeprazole (50%), lansoprazole (40%) and ranitidine (45%).

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“…Hence, acid suppression by omeprazole is a common practice to control gastroduodenal lesions (2,5). Suppression of intragastric acid also helps in the healing of ulcer (11). In animals, the role of acid in gastric lesions has been studied using some animal models such as stress or nonsteroidal antiinflammatory drug-induced gastric ulcer.…”

mentioning

confidence: 99%

A Novel Antioxidant and Antiapoptotic Role of Omeprazole to Block Gastric Ulcer through Scavenging of Hydroxyl Radical

Biswas¹,

Bandyopadhyay²,

Chattopadhyay³

et al. 2003

Journal of Biological Chemistry

255

199

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The mechanism of the antiulcer effect of omeprazole was studied placing emphasis on its role to block oxidative damage and apoptosis during ulceration. Dose-response studies on gastroprotection in stress and indomethacin-induced ulcer and inhibition of pylorus ligation-induced acid secretion indicate that omeprazole significantly blocks gastric lesions at lower dose (2.5 mg/kg) without inhibiting acid secretion, suggesting an independent mechanism for its antiulcer effect. Time course studies on gastroprotection and acid reduction also indicate that omeprazole almost completely blocks lesions at 1 h when acid inhibition is partial. The severity of lesions correlates well with the increased level of endogenous hydroxyl radical ( ⅐ OH), which when scavenged by dimethyl sulfoxide causes around 90% reduction of the lesions, indicating that ⅐ OH plays a major role in gastric damage. Omeprazole blocks stress-induced increased generation of ⅐ OH and associated lipid peroxidation and protein oxidation, indicating that its antioxidant role plays a major part in preventing oxidative damage. Omeprazole also prevents stress-induced DNA fragmentation, suggesting its antiapoptotic role to block cell death during ulceration. The oxidative damage of DNA by ⅐ OH generated in vitro is also protected by omeprazole or its analogue, lansoprazole. Lansoprazole when incubated in a ⅐ OH-generating system scavenges ⅐ OH to produce four oxidation products of which the major one in mass spectroscopy shows a molecular ion peak at m/z 385, which is 16 mass units higher than that of lansoprazole (m/z 369). The product shows no additional aromatic proton signal for aromatic hydroxylation in 1 H NMR. The product absorbing at 278 nm shows no alkaline shift for phenols, thereby excluding the formation of hydroxylansoprazole. The product is assigned to lansoprazole sulfone formed by the addition of one oxygen atom at the sulfur center following attack by the ⅐ OH. Thus, omeprazole plays a significant role in gastroprotection by acting as a potent antioxidant and antiapoptotic molecule.

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Is there an optimal degree of acid suppression for healing of duodenal ulcers?

Cited by 311 publications

References 13 publications

Effect of Omeprazole on Regional and Temporal Variations in Intragastric Acidity

Effect of Omeprazole on Regional and Temporal Variations in Intragastric Acidity

Age‐dependent eradication of Helicobacter pylori with dual therapy

A Novel Antioxidant and Antiapoptotic Role of Omeprazole to Block Gastric Ulcer through Scavenging of Hydroxyl Radical

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